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Dementia

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Dementia
SpecialtyPsychiatry, neurology Edit this on Wikidata
Frequency3.8—4% (Asia), 6.1—6.3% (Europe), 6.4—6.6% (Americas), 2.5—2.7% (Africa)
For other uses, see Dementia (disambiguation).

Dementia (from Latin de- "apart, away" + mens (genitive mentis) "mind") is the progressive decline in cognitive function due to damage or disease in the brain beyond what might be expected from normal aging.

Particularly affected areas may be memory, attention, language, and problem solving. Especially in the later stages of the condition, affected persons may be disoriented in time (not knowing what day of the week, day of the month, month, or even what year it is), in place (not knowing where they are), and in person (not knowing who they are).

Symptoms of dementia can be classified as either reversible or irreversible depending upon the etiology of the disease. Less than 10 percent of cases of dementia have been reversed. Dementia is a non-specific term encompassing many disease processes, just as fever is attributable to many etiologies.

Without careful assessment, delirium can easily be confused with dementia and a number of other psychiatric disorders because many of the signs and symptoms are also present in dementia (as well as other mental illnesses including depression and psychosis).[1]

Epidemiology

The prevalence of dementia is rising as the global life expectancy is rising. Particularly in Western countries, there is increasing concern about the economic impact that dementia will have in future, older populaces. In Australia, the 2006 estimated prevalence of dementia is 1.03% of the population as a whole. Though reports of some of the longest living people claim them to be free of it (e.g. Yone Minagawa), it is a disease which is strongly associated with age; 1% of those aged 60-65, 6% of those aged 75-79, and 45% of those aged 95 or older suffer from the disease.[2]

Diagnosis

Proper differential diagnosis between the types of dementia (see below) will require, at the least, referral to a specialist, e.g. a geriatric internist, geriatric psychiatrist, neurologist, neuropsychologist or geropsychologist. However, there are some brief (5-15 minutes) tests that have good reliability and can be used in the office or other setting to evaluate cognitive status. Examples of such tests include the abbreviated mental test score (AMTS), the mini mental state examination (MMSE), and the clock drawing test [3].

The U.S. Preventive Services Task Force (USPSTF) reviewed tests for cognitive impairment and concluded [4]:

  • MMSE
sensitivity 71% to 92%
specificity 56% to 96%

A copy of the MMSE can be found in the appendix of the original publication.[5]

Many other tests have been studied [6][7] [8] including the clock-drawing test example form). Although some may emerge as better alternatives to the MMSE, presently the MMSE is the best studied. However, access to the MMSE is now limited by enforcement of its copyright ( details).

An AMTS score of less than six (out of a possible score of ten) and an MMSE score under 24 (out of a possible score of 30) suggests a need for further evaluation. Scores must be interpreted in the context of the person's educational and other background, and the particular circumstances (for example, a person in great pain will not be expected to do well on many tests of mental ability).

Further evaluation includes retesting at another date, and administration of other (and sometimes more complex) tests of mental function, such as formal neuropsychological testing. Routine blood tests are also usually performed to rule out treatable causes. These tests include vitamin B12, folic acid, thyroid-stimulating hormone (TSH), C-reactive protein, full blood count, electrolytes, calcium, renal function and liver enzymes. Abnormalities may suggest vitamin deficiency, infection or other problems that commonly cause confusion or disorientation in the elderly. Chronic use of substances such as alcohol can also predispose the patient to cognitive changes suggestive of dementia.

A CT scan or magnetic resonance imaging (MRI scan) is commonly performed, although these modalities (as is noted below) may not have optimal sensitivity for the diffuse metabolic changes associated with dementia in a patient who shows no gross neurological problems (such as paralysis or weakness) on neurological exam. CT or MRI may suggest normal pressure hydrocephalus, a potentially reversible cause of dementia, and can yield information relevant to other types of dementia, such as infarction (stroke) that would point at a vascular type of dementia. Recently, the functional neuroimaging modalities of SPECT and PET have shown quite similar ability to diagnose dementia as clinical exam (PMID 16785801). SPECT's ability to differentiate vascular type from Alzheimer disease types of dementias appears to be superior to clinical exam (PMID 15545324).

The final diagnosis of dementia is made on the basis of the clinical picture, increasingly with neuroimaging results for backup. For research purposes, the diagnosis depends on both a clinical diagnosis and a pathological diagnosis (i.e., based on the examination of brain tissue, usually from autopsy).

Types

Cortical dementias

Subcortical dementias

  • Dementia not otherwise specified (used in cases where no specific criteria is met)

Treatment

Except for the treatable types listed above, there is no cure to this illness, although scientists are progressing in making a type of medication that will slow down the process. Cholinesterase inhibitors are often used early in the disease course. Cognitive and behavioral interventions may also be appropriate. Educating and providing emotional support to the caregiver (or carer) is of importance as well (see also elderly care).

A Canadian study found that a lifetime of bilingualism has a marked influence on delaying the onset of dementia by an average of four years when compared to monolingual patients. The researchers determined that the onset of dementia symptoms in the monolingual group occurred at the mean age of 71.4, while the bilingual group was 75.5 years. The difference remained even after considering the possible effect of cultural differences, immigration, formal education, employment and even gender as influences in the results. [9]

Snoezelen rooms that provide patients with a soothing and stimulating environment of light, color, music and scent have been used in the therapy of dementia patients.

Medications

Tacrine (Cognex), donepezil (Aricept), galantamine (Reminyl), and rivastigmine (Exelon) are approved by the United States Food and Drug Administration (FDA) for treatment of dementia induced by Alzheimer disease. They may be useful for other similar diseases causing dementia such as Parkinsons or vascular dementia.[10]

  • N-methyl-D-aspartate Blockers

Drugs within the class known as N-methyl-D-aspartate (NMDA) blockers include memantine (Namenda), which has been approved by the FDA for the treatment of moderate-to-severe dementia.

Off label

  • Amyloid deposit inhibitors

Minocycline and Clioquinoline, antibiotics, may help reduce amyloid deposits in the brains of persons with Alzheimer disease.[11]

  • Antipsychotic drugs

Haloperidol (Haldol), risperidone (Risperdal), olanzapine (Zyprexa), and quetiapine (Seroquel) are frequently prescribed to help manage psychosis and agitation. Treatment of dementia-associated psychosis or agitation is intended to decrease psychotic symptoms (for example, paranoia, delusions, hallucinations), screaming, combativeness, and/or violence.[12][13]

Depression is frequently associated with dementia and generally worsens the degree of cognitive and behavioral impairment. Antidepressants may be helpful in alleviating cognitive and behavior symptoms by reuptaking neurotransmitter regulation through reuptake of serotonin, noradrenaline and dopamine.

  • Antianxiety drugs

Many patients with dementia experience anxiety symptoms. Although benzodiazepines like diazepam (Valium) have been used for treating anxiety in other situations, they are often avoided because they may increase agitation in persons with dementia or are too sedating. Buspirone (Buspar) is often initially tried for mild-to-moderate anxiety.

Selegiline, a drug used primarilly in the treatment of Parkinson's disease, appears to slow the development of dementia. Selegiline is thought to act as an antioxidant, preventing free radical damage. However, it also acts as a stimulant, making it difficult to determine whether the delay in onset of dementia symptoms is due to protection from free radicals or to the general elevation of brain activity from the stimulant effect.

Prevention

Main article: Prevention of dementia

Since there is no cure for dementia, the best an individual can do is to prevent it from developing in the first place.

The main method to prevent dementia is to live an active life, both mentally and physically. It appears that the regular moderate consumption of alcohol (beer, wine or distilled spirits) may reduce risk. [14]

Furthermore, there are medications which might contribute to prevent the onset of dementia, including hypertension medications, anti-diabetic drugs and NSAIDs[15].

References

  1. ^ American Family Physician, March 1, 2003 Delirium
  2. ^ "Dementia Estimates and Projections: Australian States and Territories" (PDF). Alzheimer's Australia. 2005-02-01. Retrieved 2006-10-04. {{cite web}}: Check date values in: |date= (help)
  3. ^ Royall, D.; Cordes J.; & Polk M. (1998). "CLOX: an executive clock drawing task". J Neurol Neurosurg Psychiatry. 64 (5): 588–94. PMID 9598672.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  4. ^ Boustani, M.; Peterson, B.; Hanson, L.; Harris, R.; & Lohr, K. (2003). "Screening for dementia in primary care: a summary of the evidence for the U.S. Preventive Services Task Force". Ann Intern Med. 138 (11): 927–37. PMID 12779304.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  5. ^ Folstein MF, Folstein SE, McHugh PR (1975). ""Mini-mental state". A practical method for grading the cognitive state of patients for the clinician". Journal of psychiatric research. 12 (3): 189–98. doi:10.1016/0022-3956(75)90026-6. PMID 1202204.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  6. ^ Sager, M.; Hermann, B.; La Rue, A.; & Woodard, J. (2006). "Screening for dementia in community-based memory clinics". WMJ. 105 (7): 25–9. PMID 17163083.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  7. ^ Fleisher, A.; Sowell B.; Taylor C.; Gamst A.; Petersen R.; & Thal L. "Clinical predictors of progression to Alzheimer disease in amnestic mild cognitive impairment". Neurology. PMID 17287448.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  8. ^ Karlawish, J. & Clark, C. (2003). "Diagnostic evaluation of elderly patients with mild memory problems". Ann Intern Med. 138 (5): 411–9. PMID 12614094.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  9. ^ "Bilingualism Has Protective Effect In Delaying Onset Of Dementia By Four Years, Canadian Study Shows". Medical News Today. 2007-01-11. Retrieved 2007-01-16. {{cite web}}: Check date values in: |date= (help)
  10. ^ Lleo A, Greenberg SM, Growdon JH. Current pharmacotherapy for Alzheimer's disease.Annu Rev Med. 2006;57:513-33. Review. PMID 16409164
  11. ^ Choi, Y., Kim, H.S., Shin, K.Y., Kim, E.M., Kim, M., Kim, H.S., Park, C.H., Jeong, Y.H., Yoo, J., Lee, J.P., Chang K.A., Kim S., & Suh, Y.H. Related Minocycline Attenuates Neuronal Cell Death and Improves Cognitive Impairment in Alzheimer's Disease Models. Neuropsychopharmacology. 2007 Apr 4; PMID 17406652
  12. ^ Wei, Z., Mousseau, D.D., Dai, Y., Cao, X., Li, X.M. (2006). Haloperidol induces apoptosis via the sigma2 receptor system and Bcl-XS. Pharmacogenomics J. 6(4):279-88. Epub 2006 Feb 7. PMID 16462815
  13. ^ Wang, H., Xu, H., Dyck, L.E., & Li, X.M. (2005). Olanzapine and quetiapine protect PC12 cells from beta-amyloid peptide(25-35)-induced oxidative stress and the ensuing apoptosis. Journal Neuroscience Res, 81(4):572-80. PMID 15948179
  14. ^ Mulkamal, K.J., et al. Prospective study of alcohol consumption and risk of dementia in older adults. Journal of the American Medical Association, 2003 (March 19), 289, 1405-1413; Ganguli, M., et al. Alcohol consumption and cognitive function in late life: A longitudinal community study. Neurology, 2005, 65, 1210-12-17; Huang, W., et al. Alcohol consumption and incidence of dementia in a community sample aged 75 years and older. Journal of Clinical Epidemiology, 2002, 55(10), 959-964; Rodgers, B., et al. Non-linear relationships between cognitive function and alcohol consumption in young, middle-aged and older adults: The PATH Through Life Project. Addiction, 2005, 100(9), 1280-1290; Anstey, K. J., et al. Lower cognitive test scores observed in alcohol are associated with demographic, personality, and biological factors: The PATH Through Life Project. Addiction, 2005, 100(9), 1291-1301; Espeland, M., et al. Association between alcohol intake and domain-specific cognitive function in older women. Neuroepidemiology, 2006, 1(27), 1-12; Stampfer, M.J., et al'. Effects of moderate alcohol consumption on cognitive function in women. New England Journal of Medicine, 2005, 352, 245-253; Ruitenberg, A., et al. Alcohol consumption and risk of dementia: the Rotterdam Study. Lancet, 2002, 359(9303), 281-286; Scarmeas, N., et al. Mediterranean diet and risk for Alzheimer’s disease. Annals of Neurology, 2006 (published online April 18, 2006).
  15. ^ West Virginia Department of Health and Human Resources (with further links to experiments respectively)


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